Expression of cytokine genes or proteins and signaling molecules in lymphocytes associated with human ovarian carcinoma.
Int J Cancer
; 68(3): 276-84, 1996 Nov 04.
Article
en En
| MEDLINE
| ID: mdl-8903466
We have reported that tumor-associated T or natural killer (NK) lymphocytes purified from ascites of women with ovarian carcinoma show defective expression and function of signaling proteins, including reduced expression of TcR-zeta chains and p56(lck). In this study, the cytokine profiles of both tumor cells and tumor-associated lymphocytes (TAL) recovered from the tumor milieu were examined. Expression of cytokine genes was studied by semi-quantitative RT-PCR and Southern hybridization, and the presence of intracellular cytokine proteins was confirmed by immunostaining. Levels of mRNA encoding the cytokine genes typically transcribed in activated T lymphocytes, including IFN-gamma, IL-2 and IL-4, were markedly reduced, as was expression of the corresponding proteins, in TAL-T or TAL-NK cells relative to normal PBL-T or PBL-NK cells, respectively. Levels of TGF-beta and IL-6 were unaltered, while those of IL-10 were up-regulated. Although both tumor cells and TALs contributed to the enhanced level of IL-10 expression, a higher proportion of TAL-T lymphocytes than normal PBL-T cells expressed IL-10 protein. The altered profile of cytokine genes and proteins in TALs, TAL-T or TAL-NK cells was associated with impaired expression and/or function of signaling molecules, zeta chain and p56(lck). Our data suggest that abnormalities in signal transduction commonly seen in lymphocytes obtained from the tumor micro-environment are related to the concomitantly observed altered patterns of expression of cytokine transcripts and proteins.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Neoplasias Ováricas
/
Señales de Clasificación de Proteína
/
Citocinas
/
Linfocitos Infiltrantes de Tumor
Tipo de estudio:
Risk_factors_studies
Límite:
Adult
/
Aged
/
Female
/
Humans
/
Middle aged
Idioma:
En
Revista:
Int J Cancer
Año:
1996
Tipo del documento:
Article
País de afiliación:
Estados Unidos
Pais de publicación:
Estados Unidos